On Mon, 27 Sep 1999, Jeff Ricker went:
> Im sure I could get on medline or other such services and get some
> information, but I just don't have the time and I am hoping that someone
> already has a quick answer. Is there any double-blind experimental
> evidence that gingko improves performance on measures of memory (of
> whatever kind)? A student asked this question in class today.
For people with cerebrovascular disease (who benefit from ginkgo's
enhancement of blood flow to the brain), yes, there is such evidence.
But in healthy college students, nah. The last time I checked was two
years ago, but I bet nothing's changed.
On the other hand, I did find something provocative in a recent
_Journal of Neuroscience_. You know that muzzy feeling that always
seems to come with a common cold? I ruefully refer to it as being
"stoned on interleukins" (I don't suppose it's due solely to
interleukins, but I do suppose they play a part). Well, it turns out
that interleukin 1's suppression of hippocampal activity is dependent
on the increased released of endogenous adenosine. Surely there's
only one intelligent way to respond to such a glut: when you have a
cold, block your adenosine receptors with (additional) coffee. :)
--David Epstein
[EMAIL PROTECTED]
Reference:
www.jneurosci.org/cgi/content/abstract/19/11/4238
The Journal of Neuroscience, June 1, 1999, 19(11):4238-4244
Adenosine: a Mediator of Interleukin-1 beta -Induced Hippocampal Synaptic
Inhibition
Wah Ping Luk1, 2, Yu Zhang2, Thomas D. White6, Franklin A. Lue1, 4,
Chiping Wu2, 5, Cheng-Gan Jiang1, Liang Zhang2, 3, 5, and Harvey
Moldofsky1, 4
Interleukin-1 (IL-1) is a pleotrophic cytokine implicated in a variety
of central activities, including fever, sleep, ischemic injury, and
neuromodulatory responses, such as neuroimmune, and neuroendocrine
interactions. Although accumulating evidence is available regarding
the expression pattern of this cytokine, its receptors in the CNS, and
its mechanistic profile under pathological levels, it is unclear
whether this substance modulates central neurons under physiological
concentrations. Further, in light of the functional and spatial
overlap between the adenosine and IL-1 systems, it is not known
whether these two systems are coupled. We report here that, in rat
brain slices, brief application of sub-femtomolar IL-1 beta causes a
profound decrease of glutamate transmission, but not GABAergic
inhibition, in hippocampal CA1 pyramidal neurons. This decrease by
IL-1 beta is prevented by pharmacological blockade of adenosine A1
receptors. In addition, we show that IL-1 beta failed to suppress
glutamate transmission at room temperature. Because the production and
release of adenosine in the CNS is thought to be metabolically
dependent, this observation suggests that one of the functions of IL-1
beta is to increase the endogenous production of adenosine. Together,
these data suggest for the first time that sub-femtomolar levels of
IL-1 can effectively modulate glutamate excitation in hippocampal
neurons via an adenosine-dependent mechanism.
